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Wednesday, July 9, 2014

Wait, isn't it genes that make us vote the way we do?

Astory in the Tuesday NYTimes reports that our votes for president in the US is influenced by our year of birth. Or rather, who whites vote for is influenced by when they were born, whites who don't live in the South. The story describes a model constructed by Yair Ghitza and Andrew Gelman at Columbia and published as a working paper titled "The Great Society, Reagan's Revolution, and Generations of Presidential Voting." The Times piece has a nice graphic showing the effect of birth year on a lifetime of voting.

Ghitza and Gelman write

The political events of a voter’s teenage and early adult years, centered around the age of 18, are enormously important in the formation of these long- term partisan preferences. The model is shown to be powerful, explaining a substantial amount of the macro-level voting trends of the last half century, especially for white voters and non-Southern whites in particular.

Their model is a way to explain the non-monotonic pattern of voting by age. That is, the proportion of Republican votes doesn't increase steadily as people age, for example, and young people do not overwhelmingly vote Democratic, as some analysts would suggest. Instead, the graphs of votes by age jump around, as below, and Ghitza and Gelman believe their model explains why.

Republican vote by age; Ghitza and Gelman, 2014

So, while people tend to vote as their parents voted, the stronger influence according to the model is formative events when the voter is in his or her teens and early twenties. If the country was going through good times, with a president with high approval ratings, those who were teenagers at that time will vote that president's party, on average, for the rest of their lives. And vice versa. So, people who were teenagers during the Reagan years tend to vote Republican, and those who were teenagers during the Clinton years tend to vote Democratic. The authors note that the model works best for whites in general, and non-Southern whites in particular. African Americans tend to always vote Democratic, and the data weren't good enough in early years to enable the authors to treat Hispanics separately.

So, this is sort of interesting. Does it mean that candidates are wasting their money on political advertising, and it doesn't matter whether corporations are people or not? Or is the non-trend flexibility enough to swing an election and hence worth all the PAC and other sketchy dealings candidates engage in?

But wait a minute. Weren't we told not too long ago that how we vote is genetic? Fixed before birth -- yes, we take our voting patterns from our parents, but it's hard-wired, not learned. An associate professor of political science and microbiology here at Penn State, Peter Hatemi, along with a collaborator published a paper in Trends in Genetics in 2012 reviewing evidence for genes that influence our political leanings, and how we vote. So who's right? Is it our genes, or pivotal events in our adolescence?

Does science require replication?
Replication of results is one of the standard criteria for science: if you did your work right, the idea (taught to all science students) is that anyone else who wishes to should be able, at least in principle, to replicate your result. That is routinely given as the way science automatically polices itself against bad work or fraud.

The importance of replication is currently a major issue in psychology, with heated debate about whether failures to replicate original results show that they were wrong and should be reported to the authors, and what it means for the careers of the non-replicators, and so on. But, there's less discussion about what failure to replicate might really mean.

Jason Mitchell, a social psychologist at Harvard, has written on this subject, and his paper is getting torn apart by scientists of many stripes. In essence, his argument is that scientists should not attempt to replicate other's results because failure to do so is meaningless, largely because the replicators won't be as expert at the science as the original investigators. It's understandable that scientists who routinely rely on replicability, at least in principle, would criticize Mitchell's point of view.

But there are some central, yet poorly recognized issues here. And this is not to say that we agree with Mitchell's take, just that there are issues that we don't see being discussed. First, social science is not physics, or chemistry or even biology; replication is not as straightforward when humans are the subject, not atoms that are all alike, and methodology is, well, soft. A bottle of gozillions of oxygen molecules may represent replicable phenomena since each molecule is identical, and statistical methods were largely developed for and suitable to such truly replicable phenomena. Indeed, much of chemistry and physics depend on this because the behavior of individual elements, like atoms or electrons, can't be observed directly. But this is by no means so clearly the case for social or genetic or evolutionary phenomena. We've blogged before on the imperfectability of the social sciences (e.g., here), so enough said about that.

More importantly, researchers routinely try to replicate studies in epidemiology, to identify the cause of obesity or heart disease or asthma -- and what we now know is that obesity is caused by energy imbalance or processed foods or sugar or high fructose corn syrup or the not-Mediterranean diet or gluten and much much more, including an ever-growing list of genes. And, asthma is caused by breast feeding, bottle feeding, poverty, wealth, prenatal stress, postnatal stress, antibiotics, acetaminophen and much much more, as well as an ever-growing list of genes. A tentative finding is followed-up (a favored grant strategy, in fact) with larger samples to try to refine the estimates of effects -- assuming the effects are still there!

In fact, genetic and epidemiological studies of complex diseases often fail to replicate earlier studies, which is why we so often see science news stories that, shockingly, overturn accepted beliefs. But it's usually not clear why a new study doesn't find the same as an earlier one, and sometimes can't be clear. It's too easy to say that things weren't measured as accurately etc. in the previous study -- or the replicating study -- but that is often not a very convincing explanation. There are many pathways to complex diseases, and people can get to the same place in their own way. So, two studies, though they yield different results, might well be correct. But how would we know? Replicate again? Two out of three? Toss a coin? Take a vote of 'experts'?

A sample involving complex living organisms -- mice, humans, ferrets -- is never possible to completely replicate. Because we're the result of evolution, which is about diversity, we are simply never the same. Even the same investigators, using the same equipment run by the same technicians in the same lab may fail to replicate their own earlier results if they are analyzing samples from different study populations. Or even a second sample of the same people at a later time, or different people from the same population. People aren't atoms. If an effect is small, its detectability or net effect may depend on the presence and frequency of other causal factors in a given sample. Even a positive replication may be for differing reasons (more than one cause for a similar outcome, a different mix in different samples). So failure to replicate need not mean a suspected cause isn't a cause after all -- it may reflect a poor understanding of evolution and variation. We do not have an adequate body of theory for understanding the specifics of given cases, even in genetics and certainly in social sciences.

P.S. Our vote on the voting studies
For what it's worth, we wouldn't bet on either of the explanations for how we vote, replicated or not. The pivotal-events hypothesis is as unlikely to actually explain voting as is the political-genetics hypothesis, largely because both are attempting to reduce a complex, population-level trait to simple, single explanations. And then apply them to individuals -- there's a name for this; it's called the ecological fallacy. As with complex diseases, there surely isn't a one-to-one relationship (Ghitza and Gelman no doubt would agree, given that they don't find the same results for African Americans, and the effect is stronger outside the Southern US); there are many paths to how people vote, and how people vote can change over time.

And despite what behavioral geneticists claim, we don't know nearly enough about genetics to be able to attribute a culturally laden trait like voting preference to genes. Political preference can cluster in families and appear genetic for a variety of reasons, and we know that voting patterns are transitory.

So, pardon us if we don't take seriously either model of what makes us vote the way we do. Maybe we need to fix up social science, and maybe some people who do 'genetics' ought to have a better understanding of genetics, before we start making assertions about cause, by confusing correlation with causation, and temporary patterns as if they were inherent.

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